Analysis of related complications of totally implantable venous access ports in children's chemotherapy: Single center experience.

Totally implantable venous access port (TIVAP) has become an important infusion channel for children who need chemotherapy. With the popularization of TIVAP, its related complications have gradually received clinical attention. However, there are few studies on the complications of TIVAP in children. Therefore, this study intends to analyze the risk factors of complications in children's infusion port, so as to provide basis for guiding clinical prevention and intervention. This paper retrospectively analyzed 182 children who received TIVAP implantation in our hospital from January 2018 to January 2021. According to the demographic data, basic disease status and operation related data obtained through Hospital Information System and manual follow-up, the complications and related influencing factors after implantation and implantation were summarized and analyzed. SPSS software was used to analyze the influencing factors between the complication group and the control group. There were 182 cases of children implanted in intravenous infusion port, of which 71 cases had complications, infection was the most common complication in 50 cases, followed by catheter blockage in 23 cases. Among the infection factors, catheter-related blood stream infection accounted for the highest proportion in 31 cases (17.0%), and Staphylococcus epidermidis was the most common pathogen. A total of 19 cases were pulled out early, and the unplanned pullout rate of catheter-related blood stream infection was the highest. In the analysis of influencing factors, age had significant differences in catheter-related infection, all complications and no complications (P < .05). The overall incidence of complications in the use of TIVAP in children with chemotherapy is high, and infection is the most common complication, among which catheter-related blood stream infection is the most common cause of unplanned pullout. Lower age may be associated with a higher incidence of complications.

FOXP2 regulates thyroid cancer cell proliferation and apoptosis via transcriptional activation of RPS6KA6.

The transcription factor, forkhead box P2 (FOXP2) has tumor-suppressive effects in several types of cancer. However, the regulatory role and underlying mechanism of FOXP2 in thyroid cancer (THCA) is not completely understood. In the present study, the mRNA expression levels of FOXP2 and ribosomal protein S6 kinase A6 (RPS6KA6) were evaluated using the GEPIA database and THCA cell lines. The association between FOXP2 and RPS6KA6 was analyzed using the LinkedOmics, and GEPIA databases. Then, the binding sites of FOXP2 and the RPS6KA6 promotor was predicted using the JASPAR database, and verified using a dual-luciferase reporter assay and chromatin immunoprecipitation. In addition, functional assays investigating FOXP2 and RPS6KA6 were conducted in the TPC-1 cell line. The data showed that FOXP2 and RPS6KA6 mRNA expression levels were decreased in the THCA tissues, and cell lines. Overexpression of FOXP2 inhibited cell proliferation and promoted apoptosis in the THCA cell lines. Furthermore, RPS6KA6 mRNA expression levels were reduced in THCA and were correlated with FOXP2 expression level. Mechanistic studies revealed that FOXP2 binds directly to the promotor region of RPS6KA6 and modulated the expression level of RPS6KA6 transcriptionally. In addition, rescue experiments showed that knockdown of RPS6KA6 expression reversed the effects of FOXP2 overexpression on THCA cell proliferation and apoptosis, and the regulation of FOXP2/RPS6KA6 may be associated with the PI3K/AKT pathway. In summary, FOXP2 was associated with the proliferation and apoptosis of human THCA cells via the transcriptional activation of RPS6KA6. The FOXP2/RPS6KA6 axis could be a promising target for the treatment of THCA.

Knockdown of miR-194-5p inhibits cell proliferation, migration and invasion in breast cancer by regulating the Wnt/ß-catenin signaling pathway.

Breast cancer is a major public health concern, due to its increasing incidence and limited effective treatment. The present study aimed to investigate the expression of microRNA (miR)­194­5p and its roles in breast cancer. The expression levels of miR­194­5p and SRY­box 17 (SOX17) mRNA were detected in breast cancer tissues and cell lines by reverse transcription­quantitative polymerase chain reaction. The protein expression levels were determined by western blotting. In addition, MTT, colony formation, scratch and Transwell assays were use to evaluate the characteristics of MCF­7 cells with miR­194­5p knockdown. The target verification of miR­194­5p was determined by luciferase reporter assay. Furthermore, tumor­bearing nude mice with miR­194­5p knockdown were used to assess the effects of miR­194­5p on tumor activity. In breast cancer tissues, miR­194­5p was upregulated, whereas SOX17 was downregulated. In addition, the expression levels of SOX17 and phosphorylated (p)­ß­catenin in the cytosol and nucleus were increased in the miR­194­5p inhibitor group. In addition, cell proliferation, migration and invasion were inhibited in response to miR­194­5p knockdown. The luciferase reporter assay confirmed that SOX17 was a target gene of miR­194­5p. In the mouse studies, knockdown of miR­194­5p suppressed tumor growth and promoted SOX17 expression in nude mice with breast cancer. These findings suggested that knockdown of miR­194­5p may increase the expression of SOX17 and regulate the Wnt/ß­catenin signaling pathway in breast cancer cells; therefore, miR­194­5p may be considered a potential target for breast cancer prevention.

Total parathyroidectomy with forearm auto-transplantation improves the quality of life and reduces the recurrence of secondary hyperparathyroidism in chronic kidney disease patients.

BACKGROUND: Our study aims to explore the effect of total parathyroidectomy (PTX) with forearm autotransplantation (FAT) on the quality of life and recurrence of secondary hyperparathyroidism (SHPT) in chronic kidney disease patients. METHODS: A total of 104 chronic kidney disease patients with SHPT were enrolled and divided into the PTX (n = 62) and PTX + FAT (n = 42) groups. The operation efficacy was evaluated by analyzing preoperative and postoperative values, including levels of intact parathyroid hormone (iPTH), serum phosphorus, serum calcium, alkaline phosphatase (ALP), calcium-phosphorus product, signs and symptoms, and MOS 36-item short-form health survey (SF-36) scores. Moreover, complications and recurrences were followed up for 12 months after the operation. Binary logistic regression was to present the risk factors for the recurrence of chronic kidney disease patients with SHPT. RESULTS: Compared with the preoperative values, the PTX and PTX + FAT groups showed decrease postoperative levels of iPTH, serum phosphorus, serum calcium, calcium-phosphorus product, bone pain, and skin pruritus at all time periods. The PTX and PTX + FAT groups demonstrated decreased ALP, fracture or deformity, and coronary artery calcification at 1 month, decreased short stature at 3 months after the operation but increased SF-36 score after operation. Compared with the PTX group, the level of iPTH decreased and the levels of serum calcium, calcium-phosphorus product increased at 3, 6, and 12 months after the operation in the PTX + FAT group. The levels of ALP, fracture or deformity, short stature, and SF-36 decreased separately at 1 week and 6 and 12 months after the operation, along with the decrease of coronary artery calcification and the recurrence rate, respectively, at 6 and 12 months after the operation in the PTX + FAT group when compared with those in the PTX group. Logistic regression analysis evidenced that the preoperative iPTH level, SF-36 score, and operation type were the risk factors for the recurrence of chronic kidney disease with SHPT. CONCLUSION: Total PTX combined with FAT is more effective in improving the quality of life and reducing the recurrence of chronic kidney disease with SHPT than PTX alone.

The Efficacy of Rituximab Combined with 131I for Ophthalmic Outcomes of Graves' Ophthalmopathy Patients.

PURPOSE: The purpose of this study is to examine the effectiveness of introducing both rituximab (RTX) and 131I for active Graves' ophthalmopathy (GO) with hyperthyroidism. METHODS: In total, 217 patients suffering from active GO with hyperthyroidism were included in this research. All subjects were randomly assigned to 3 groups. Patients in group A solely received 131I treatment; group B1 underwent a methylprednisolone treatment in combination with 131I treatment; and group B2 received an RTX in combination with 131I treatment. Hyperthyroidism treatment outcomes, orbital volumetry, ophthalmic assessments, serum cytokine levels, and adverse effects were measured after treatment. RESULTS: The orbital volumetry principle was significantly different from 24 weeks after the start of treatment among all 3 groups, and improvements in most ophthalmic parameters were regarded significantly different among 3 groups (all p < 0.05). The expression levels of miR-146a and most serum cytokines were regarded significantly different from 24 weeks after the start of treatment among 3 groups (all p < 0.05). CONCLUSIONS: In comparison with other therapies, RTX treatment in combination with 131I treatment is considered to be more effective for hyperthyroidism with active GO.

GSTT1 polymorphism and breast cancer risk in the Chinese population: an updated meta-analysis and review.

BACKGROUND: Although a number of studies have been conducted on the association between GSTT1 polymorphism and breast cancer in China, this association remains elusive and controversial. To clarify the effects of GSTT1 polymorphism on the risk of breast cancer, an updated meta-analysis was performed in the Chinese population. MATERIAL/METHODS: Related studies were identified from PubMed, Springer Link, Ovid, Chinese Wanfang Data Knowledge Service Platform, Chinese National Knowledge Infrastructure (CNKI), and Chinese Biology Medicine (CBM) to up 28(th) January 2015. Pooled ORs and 95% CIs were used to assess the strength of the associations. RESULTS: A total of 13 studies including 3387 breast cancer cases and 5085 controls were involved in this meta-analysis. Overall, a significant association (OR = 1.31, 95% CI: 1.02-1.67) was found between the null GSTT1 and breast cancer risk when all studies in Chinese population pooled into the meta-analysis. In subgroup analyses stratified by geographic areas and source of controls, it revealed the significant results in population-based studies (OR = 1.42, 95% CI: 1.23-1.65) and South China (OR = 1.47, 95% CI: 1.27-1.70). CONCLUSIONS: This meta-analysis showed that the null GSTT1 may be potential biomarkers for breast cancer risk in Chinese, and further studies with gene-gene and gene-environment interactions are required for definite conclusions.

[Immunological killing effect of recombicant adenovirus vector rAD-mTERT-m4-1BBL on mouse hepatoma cell line Hepa1-6 cells co-cultured with T lymphocytes].

OBJECTIVE: To study the immunological suppressing effect of recombinant adenovirus vector rAD-mTERT promotor-m4-1BBL (rAD-mTERT) on mouse hepatoma cell line Hepa1-6 cells in co-culture with T lymphocytes. METHODS: Adding recombinant adenovirus rAD, rAD-CMV-m4-1BBL (rAD-CMV) and rAD-mTERT to Hepa1-6 and L929 cells, respectively, to observe the effect of these adenoviruses on growth and apoptosis of these cells in co-culture with T lymphocytes. RESULTS: Adding adenovirus significantly suppressed the growth and slightly increased apoptosis of the two types of cells (P < 0.05). rAD-mTERT promotor-m4-1BBL showed only pro-apoptotic effect on Hepa1-6 cells. When co-cultured with T lymphocytes, rAD-CMV-m4-1BBL showed promoting effect on apoptosis of the cells. Compared with that of T cells pre-co-culture, CD4(+) and CD8(+) T cells were proliferated, and the ratio of CD4/CD8 was significantly reduced (from 1.27 to 1.08). CONCLUSION: Adding the recombinant adenoviruses only suppresses the cell growth, but not promotes their apoptosis. In co-culture with T lymphocytes, recombinant adenovirus vector rAD-mTERT promotor-m4-1BBL can targetingly suppress the growth and induce apoptosis of Hepa1-6 cells. The apoptosis is induced through the immunological killing effect of T lymphocytes.